Pharm: some anti hypertensives & anti-anginals Flashcards Preview

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Flashcards in Pharm: some anti hypertensives & anti-anginals Deck (20):

How do you treat HTN in CHF? Special considerations

use diuretics, ARBs/ACE-Is, beta blockers in compensated CHF, and aldosterone inhibitors. Beta blockers are contraindicated in cardiogenic shock and must be used very cautiously in decompensated CHF.


How do calcium channel blockers work?

calcium channel blockers block the voltage-gated L-type calcium channels in heart and smooth musle. this reduces the contractility.


How do different CCBs rank in terms of their effects on vascular smooth muscle?

amlodipine = nifidepine > diltiazem > verapamil


Clinical uses of amlodipine and nifedipine

used to treat HTN and angina and vasospastic conditions, including Raynauds and Prinzmetal angina
both are dihydropyridines (plus nimodipine)


Clinical use of nimodipine?

treats subarachnoid hemorrhage by preventing cerebral vasospasm.


clinical use of diltiazem and verapamil

used to treat HTN, angina, and atrial fibrillation/flutter


CCB toxicity

cardiac depression, AV node block, peripheral edema, constipation (relaxes smooth muscle), hyperprolactinemia


How does hydralazine work?

hydralazine incr. cGMP, which causes smooth muscle relaxation. this will affect arterioles more than veins and reduces AFTERLOAD.


When is hydralazine used? Special considerations?

hydralazine is the FIRST LINE for HTN in pregnancy. It can cause a reflex tachycardia as it drops blood pressure and thus is contraindicated in CAD/angina. We usually prescribe this with a beta blocker to reduce reflex tachycardia


What are the toxicities of hydralazine?

causes a compensatory tachycardia and is contraindicated in CAD and angina. it can also cause a LUPUS-LIKE SYNDROME. May also cause fluid retention, nausea, headache, angina (won't stress if I don't get these last 4).


What is a hypertensive emergency?

Systolic >210; diastolic > 120, esp. with end organ damage


There are many drugs used to treat a hypertensive emergency. Which two will I know?

nitroprusside and fenoldopam


How does nitroprusside work?

It increases cGMP via direct release of NO. this is short acting.


How does fenoldopam work?

this is a D1 receptor agonist. It causes coronary, renal, and splanchnic vasodilation to decr. BP and incr. naturiesis


How do different CCBs rank in terms of their effects on the heart?

verapamil > diltiazem > amlodipine/nifedipine (verapmil = ventricle). opposite order when compared with effects on vascular smooth muscle.


How do does nitroglycerin work? What is another drug that works in the same way?

both nitroglycerin and isosorbide dinitrate incr. NO in vascular smooth muscle. This increases cGMP and causes smooth muscle relaxation. nitrates dilate veins >>> arteries and reduce preload.


What is "Monday disease?"

seen in patients who have industrial exposure to nitrates. these patients develop tolerance during the week and loose it on the weekend. At work again on Monday, they experience tachycardia, dizziness, and headache on re-exposure.


Nitroglycerin toxicity

hypotension, reflex tachycardia that can be prevented with beta blockers, flushing, and headache.


nitroglycerin use

angina, acute coronary syndrome, and pulmonary edema (to decr. preload?)


Anti anginal therapy: look at nitrates, beta blockers, and combination wrt end-diastolic vol, BP, contractility, HR, ejection time, and myocardial O2 consumption

nitrates: decrease preload. end diastolic vol decr., BP decr. contractility incr (reflex), HR incr. (reflex), ejection time decr. (I think of this as a reflex), O2 consumption decr.
beta blockers: decr. afterload. end-diastolic vol incr. (more time to fill), BP decr, contractility decr., HR decr. ejection time incr., O2 consumption decr.
no effect or decr. EDV, BP decr., little to no effect on contractility, decr. HR, little to no effect on ejection time, and more decreased myocardial O2 consumption.